Compositions and methods for the prevention and treatment of cardiovascular diseases

ABSTRACT

Compositions comprising electro-activated aqueous solutions and methods for the prevention and treatment of dysfunctional cardiovascular conditions are provided.

CROSS REFERENCE TO RELATED APPLICATIONS

This application is a divisional of U.S. patent application Ser. No.13/055,691, which was filed Apr. 14, 2011, and was a 371 National Stagefiling of PCT/US2009/051694, which was filed Jul. 24, 2009, and claimsthe benefit of U.S. Provisional Patent Application Ser. No. 61/129,883,which was filed Jul. 25, 2008, all of which are incorporated byreference as if fully set forth.

BACKGROUND OF THE INVENTION

Cardiovascular diseases, which include coronary heart disease (heartattacks), cerebrovascular disease, raised blood pressure (hypertension),peripheral artery disease, rheumatic heart disease, congenital heartdisease and heart failure, derive from dysfunctional conditions of theheart, arteries, and veins that supply oxygen to vital life-sustainingorgans, including the brain and the heart itself. Major causes ofcardiovascular disease are tobacco use, physical inactivity and anunhealthy diet.

Heart attacks and strokes are mainly caused by a blockage in the innerwalls of the blood vessels that prevents blood from flowing to the heartor the brain. Arteriosclerosis and atherosclerosis are excess buildup offat or plaque deposits, respectively, that cause narrowing of the veinsthat supply oxygenated blood to the heart and may lead to ischemic heartdisease, an obstruction of blood flow to the heart. Excess fat or plaquebuildup may also cause high blood pressure (hypertension), a diseaseknown as “The Silent Killer” because the first warning sign is an anginaattack, a deadly heart attack or a stroke. Kidney disorders, obesity,diabetes, smoking, excess alcohol, stress, and thyroid and adrenal glandproblems can also exacerbate a high blood pressure condition.

Damage to the heart tissues from cardiovascular diseases or heartsurgery disrupts the natural electrical impulses of the heart andresults in cardiac arrhythmia. Sudden fluctuations in heart rate cancause cardiac irregularities and insufficiencies, includingpalpitations, supraventricular tachycardia, fibrillation faintness ordizziness, and even initiate a heart attack.

Mismatch of cardiac output during strenuous exercise may lead to muscledamage, induce fatigue and affect athletic performance.

Arteries spasm and irregular contraction and expansion of blood vesselsin the brain may reduce flow of blood from the occipital lobe andtrigger migraines.

Levels of total blood cholesterol above 250 mg/dL, LDL cholesterol above130 mg/dL (3.0 mmol/L), HDL cholesterol below 35 mg/dL andlipoprotein(a) level greater than 30 mg/dL may also lead to a heartattack or stroke.

Infections of the heart, known as carditis and endocarditis, may occuras a result of a weak immune system, liver problems, heart surgery, orfrom an autoimmune disorder like rheumatic fever.

Heavy smoking may cause Buerger's disease, also known asthrombophlebitis obliterans, an acute inflammation and thrombosis(clotting) of arteries and veins of the hands and feet, which is oftenassociated with intense pain in the extremities, claudication in thefeet and/or hands, numbness and/or tingling in the limbs, skinulcerations, gangrene and Raynaud's phenomenon, a condition in which thedistal extremities turn white upon exposure to cold.

Peripheral arterial occlusive disease may cause diabetic ulcers, whichare the most common foot injuries leading to lower extremity amputationin diabetic patients.

Often, there are no symptoms of underlying cardiovascular diseases and aheart attack or stroke may be the first warning. Early medical detectionand treatment is available, however, is not always effective.Angiograms, bypass surgery and angioplasty are invasive and traumaticprocedures associated with high cost and often requiring additionaltherapy and/or intervention.

Accordingly, there is a need in the art for improved prevention andtreatment options for cardiovascular diseases and the present inventionsatisfies this need.

SUMMARY OF THE INVENTION

It is therefore an object of the invention to provide solutions to theaforementioned deficiencies in the art.

It is an object of the present invention to provide a therapeuticcomposition for the prevention and treatment of dysfunctionalcardiovascular conditions.

It is a further object of the invention to provide a method for treatingor preventing a dysfunctional cardiovascular condition in a subject inneed thereof.

To accomplish these and other objectives, the invention provides atherapeutic composition comprising an electro-activated solution with anegative oxidation-reduction potential (ORP) in a range between −50 mVand −500 mV, a conductivity between 11 and 15 mS/cm and a pH in therange between 6.5 and 7.6.

The composition of the invention, which is prepared by mixing twoelectro-activated solutions, Solution A with a stable negativeoxidation-reduction potential, and Solution B with a stable positiveoxidation-reduction potential, prior to use, is stable for at least 48hours when stored at 4°-8° C.

Further, the invention provides a stable therapeutic compositioncomprising an electro-activated solution, which has a stable positiveoxidation-reduction potential (ORP) in the range between +500 mV and+900 mV for a period of at least 12 months when stored at 15°-25° C. inno direct sunlight, and a pH in the range between 6.5 and 7.8.

Moreover, the invention provides a stable therapeutic compositioncomprising an electro-activated solution, wherein the electro-activatedsolution has an oxidation-reduction potential (ORP) in the range between−500 mV and −900 mV for a period of at least 12 months when stored at15°-25° C. in no direct sunlight, and a pH in the range between 3.2 and4.5.

In a preferred aspect of the invention, the electro-activated solutionsof the invention comprise magnetic dipole stabilized water (MDSW). Inone aspect of the invention, the electro-activated solutions furthercomprises an organic molecule of organic molecule of the formula

wherein R1 is NH₂ and R2 is

In another aspect of the invention, the organic molecule has a longercarbon chain.

In a specific embodiment, the electro-activated solution comprises0.5-10% magnesium sulfate hexahydrate, 5.0-20.0% ascorbic acid, 0.2-2.0%niacinamide, 0.2-2% pyridoxin HCl, 0.01-2.0% calcium D pantothenate,0.1-1.0% thiamin HCl, 0.01-0.1% riboflavin, 0.001-0.1% cyanocobalamin,0.05-10% sodium lactate and 5-500 ml magnetic dipole stabilized water.

In another specific embodiment, the electro-activated solution comprises190-220 mg nicotinic acid, 9.5-11.0 mg thiamin HCl, 1.9-2.2 mgriboflavin, 285-330.0 mg folic acid, 23.7-27.5 μg cyanocobalimin,23.7-27.5 μg pyridoxin HCl, 100% magnetic dipole stabilized water,1.04-1.2 g magnesium chloride, 1.9-2.2% 2-di-ethyl amino ethanol,228-264.0 mg ascorbic acid and 0.4-0.75% amino acetic acid. In a furtheraspect of the invention, the electro-activated solution (MDSW) containsinorganic salts at an ionic concentration of 50 to 500 parts permillion. In a preferred aspect of the invention, the inorganic salts aresodium chloride, sodium bicarbonate and magnesium sulfate, and theelectro-activated solution contains 0.5-1.0 g/l of sodium bicarbonate,8.0-10.0 g/l of sodium chloride and 4.5-7.5 g/l of magnesium sulfate.

In an additional embodiment, the invention provides a method fortreating or preventing a dysfunctional cardiovascular condition in asubject in need thereof, comprising administering to the subject atherapeutic composition comprising a therapeutically effective amount ofelectro-activated solution. The electro-activated solution has anegative oxidation-reduction potential (ORP) in a range between −50 mVand −500 mV, a conductivity between 11 and 15 mS/cm and a pH in therange between 6.5 and 7.6. In a preferred aspect of the invention, theelectro-activated solution comprises magnetic dipole stabilized water(MDSW). In one aspect of the invention, the electro-activated solutionfurther comprises an organic molecule of the formula

wherein R1 is NH₂ and R2 is

In another aspect of the invention, the organic molecule has a longercarbon chain.

In a specific embodiment, the electro-activated solution comprises0.5-10% magnesium sulfate hexahydrate, 5.0-20.0% ascorbic acid, 0.2-2.0%niacinamide, 0.2-2% pyridoxin HCl, 0.01-2.0% calcium D pantothenate,0.1-1.0% thiamin HCl, 0.01-0.1% riboflavin, 0.001-0.1% cyanocobalamin,0.05-10% sodium lactate and 5-500 ml magnetic dipole stabilized water.In another specific embodiment, the electro-activated solution comprises190-220 mg nicotinic acid, 9.5-11.0 mg thiamin HCl, 1.9-2.2 mgriboflavin, 285-330.0 mg folic acid, 23.7-27.5 μg cyanocobalimin,23.7-27.5 μg pyridoxin HCl, 100% magnetic dipole stabilized water,1.04-1.2 g magnesium chloride, 1.9-2.2% 2-di-ethyl amino ethanol,228-264.0 mg ascorbic acid and 0.4-0.75% amino acetic acid. In a furtheraspect of the invention, the electro-activated solution (MDSW) containsinorganic salts at an ionic concentration of 50 to 500 parts permillion. In a preferred aspect of the invention, the inorganic salts aresodium chloride, sodium bicarbonate and magnesium sulfate, and theelectro-activated solution contains 0.5-1.0 g/l of sodium bicarbonate,8.0-10.0 g/l of sodium chloride and 4.5-7.5 g/l of magnesium sulfate.

In one aspect of the invention, the composition is administered to thesubject to be treated by parenteral injection. In preferred embodimentsof the invention, the composition is diluted in isotonic intravenous(IV) fluid and administered intra-arterially, intravenously orintra-arterially and intravenously. Following treatment, the compositionmay be administered periodically as a maintenance therapy. The subjectto be treated may have or may be at risk of having a dysfunctionalcardiovascular condition. Dysfunctional cardiovascular conditionsinclude, but are not limited to, coronary heart disease, cerebrovasculardisease, hypertension, peripheral artery disease, rheumatic heartdisease, congenital heart disease, heart failure, cardiac insufficiency,palpitations, supraventricular tachycardia, fibrillation, faintness,dizziness, fatigue, migraine, high levels of total blood cholesteroland/or high LDL cholesterol, low level of HDL cholesterol, high level oflipoprotein, carditis and endocarditis, diabetic ulcer,thrombophlebitis, Raynauds disease, claudication and gangrene.

DETAILED DESCRIPTION OF THE INVENTION

The compositions and methods of the present invention are for theprevention and treatment of dysfunctional cardiovascular conditions. Theaim of the invention is to provide effective, non-invasive methods toprevent and treat a dysfunctional cardiovascular condition in a subjectin need thereof, by restoring cellular integrity and trans membranepotential, modulating cellular membrane permeability and enhancing thetransfer of molecules and ions through the cell membranes.

The terms “subject” and “patient” are used interchangeably, and aremeant to refer to any mammal, including humans, that has, or is at riskof developing, a dysfunctional cardiovascular condition. The subject orpatient is typically human, however, other suitable subjects or patientsinclude, but are not limited to, laboratory animals, such as mouse, rat,rabbit, or guinea pig, farm animals and domestic animals or pets.Non-human primates are also included.

As used herein, a “therapeutically effective amount” is an amounteffective to elicit a cellular response that is clinically significant.

As used herein, by “dysfunctional cardiovascular conditions” it is meantto include cardiac and vasculatory malfunctions, such as coronary heartdisease, cerebrovascular disease, hypertension, peripheral arterydisease, rheumatic heart disease, congenital heart disease, heartfailure, cardiac insufficiency, palpitations, supraventriculartachycardia, fibrillation, faintness, dizziness, fatigue, migraine, highlevels of total blood cholesterol and/or LDL cholesterol, low level ofHDL cholesterol, high level of lipoprotein, infections of the heart suchas carditis and endocarditis, diabetic ulcer, thrombophlebitis, Raynaudsdisease, claudication and gangrene.

As used herein, “nicotinic acid”, “niacinamide’ and “folic acid” may beused interchangeably in the solutions and compositions of the invention.

As used herein, magnesium salts, including magnesium sulfate andmagnesium chloride, may be used interchangeably in the solutions andcompositions of the invention.

Free oxygen radicals, also known as reactive oxygen species (ROS), causemuch damage to macromolecules, including lipids, proteins and nucleicacids. One major toxic effect of oxygen radicals is damage to cellularmembranes, including the plasma, mitochondrial and endo-membranesystems, which is initiated by lipid peroxidation and is accompanied byincreased membrane rigidity, decreased activity of membrane-boundenzymes, altered activity of membrane receptors and altered membranepermeability. Furthermore, oxygen radicals can also directly attackmembrane proteins and induce lipid-lipid, lipid-protein andprotein-protein crosslinking, which in turn affects membrane function.

Because of their reactivity, free oxygen radicals may react with DNA,resulting in mutations that can adversely affect the cell cycle andpotentially lead to cancer and malignancies. Moreover, oxygen freeradicals are involved in cardiovascular diseases, the aging process,neurodegenerative diseases, including ALS, Parkinson's disease andAlzheimer's disease, cataractogenesis, atherosclerosis, diabetesmellitus, ischemia-reperfusion injury, kwashiorkor, senile- anddrug-induced deafness, schizophrenia, atherosclerosis andalcohol-induced liver damage.

There is strong evidence in the literature that free oxygen radicalsoxidize low density lipoprotein (LDL), which is then engulfed byphagocytes to form foam cells and plaques in the cardiovascular wall.These plaques harden and narrow the blood vessels and impair blood flow,thus depriving the heart of oxygen and nutrients. In addition, ischemiais often followed by reperfusion injury, which is caused by inadequatesupplies of intracellular antioxidants. Ischemia and reperfusion are amajor cause of strokes.

There is also increasing evidence that mismatch of cardiac output duringstrenuous exercise causes release of free oxygen radicals, whichcontribute to muscle damage and induce fatigue and/or injury.

Moreover, it has been reported that the activity of the anti-oxidantenzymes superoxide dismutase (SOD), catalase (CAT) and glutathioneperoxidase (GSH-Px) is significantly lower in subjects suffering frommigraine. SOD is known to protect against vasoconstriction or vasospasminduced by superoxide radicals. Migraine is a potential risk factor ormarker for atherosclerosis-related diseases.

Cardiovascular Disease

At any given time, the distribution of blood in a person's body will beapproximately:

64% veins

13% arteries

9% pulmonary vessels

7% heart

7% arterioles and capillaries.

Although the heart weighs less than 1% of the total body weight, itrelentlessly receives nearly 5% of the total blood flow (which mayexplain why the arteries of the heart can so easily develop problems).Congenital defects and infectious disease can strike anywhere, but byfar the most common disease occurs in the arteries: atherosclerosis.

Blockages can occur in veins as well as in arteries, but those in theveins tend to be caused by blood clots, or thrombi, rather than byatherosclerosis. Thrombophlebitis (or often called phlebitis) mostcommonly involves clotting of blood and inflammation of a vein in theleg. This can be serious if a portion of the clot becomes detached,travels through the heart and gets pumped to the lung where it blocks apulmonary artery as a pulmonary embolism. About 10% of people withpulmonary embolism die within an hour.

Clotting of blood in the veins can occur when blood flow is slow orstagnant. This can occur during long periods of immobilization such aswhen a person is confined to a hospital bed, cramped in a crowdedairplane on a long flight or driving for an extended period.

Atherosclerosis

Atherosclerosis (hardening of the arteries) occurs “naturally” withaging as a result of cross-linking of macromolecules like proteins andpolysaccharides. Atherosclerosis refers to the formation and hardeningof fatty plaques (atheromas) of the inner surface of the arteries. Inatherosclerosis, the arteries not only harden, they narrow, sometimesnarrowing so much that hardly any blood can get through. Such narrowsvessels are easily blocked by constriction or objects in thebloodstream.

The internal surface of an artery is covered with a single layer ofendothelial cells that are pressed against each other like flagstones ona terrace. Atherosclerosis begins with injury to endothelial cells,exposing portions of the artery surface below the endothelium. Freeradicals, chemicals in cigarette smoke or other irritants could beresponsible for the injury, as could turbulence and mechanical force dueto high blood pressure. Platelets (round cells half as large as redblood cells) clump around the injured endothelial cells and releaseprostaglandins, which cause the endothelial cells to proliferate likecancer. LDL-cholesterol particles release their fat into the areas madeporous by prostaglandins. Macrophages (scavenger white blood cells)engorge themselves on oxidized LDL-cholesterol until they becomeunrecognizable “foam cells” that invade atheromas. Then the atheromasare hardened by fibrin (which forms scar tissue) and finally by calciumpatches. A vicious circle often arises with scar tissue attracting moreplatelets and LDL-engorged macrophages.

Atherosclerotic Cardiovascular Disease

Atherosclerosis can occur in any artery. Most commonly it occurs in theaorta, the artery that receives blood directly from the heart. Since theaorta is the largest artery in the body, it is rarely criticallynarrowed by atheromas. Nonetheless, atherosclerosis can contribute toaneurysms (ballooning of an artery, responsible for only one-fortieth ofthe mortality rate of heart attack—an aortic aneurysm killed AlbertEinstein, who refused to be operated upon.) The most frequentlife-threatening problems, however, are caused by the arteries supplyingthe heart, the brain and the kidneys, in that order.

Cholesterol

Since the blood is 80% water, fats will not dissolve in the blood.Therefore, fats need to be attached to carrier molecules to travelthrough the bloodstream. The principle carrier molecules for fat arealbumin, chylomicrons, Very Low Density Lipoprotein (VLDL), Low DensityLipoprotein (LDL) and High Density Lipoprotein (HDL). Free Fatty Acids(FFAs) are attached to albumin, whereas triglycerides are mainlytransported by chylomicrons and VLDL. Cholesterol and phospholipid areprimarily transported by LDL and HDL.

Cholesterol is supplied to cells primarily by the attachment of LDL tospecific LDL receptors on cell membranes. Thyroid hormone lowers bloodcholesterol by increasing the number of LDL receptors on cells. For mostpeople, atherosclerosis due to excessive LDL-cholesterol in the blood isthe result of a high level of dietary saturated fat resulting in highLDL-cholesterol production by the liver.

The primary function of HDL seems to be to remove excess cholesterolfrom the bloodstream. LDL can directly release cholesterol into arterialareas made porous by prostaglandins—whereas HDL can scoop up this loosecholesterol and return it to the liver. Thus, HDL deficiency can be asserious an atherosclerosis risk as LDL-cholesterol excess. A 1%reduction in blood cholesterol is generally associated with a 2%reduction in risk of coronary artery disease, within “normal” levels ofblood cholesterol.

Free Fatty Acids

Free fatty acids are a major source of energy for many organs, includingthe heart. Triglycerides are hydrolyzed into FFAs and glycerol by theenzyme lipase, which is found both inside cells and on the surface ofthe endothelial cells of capillaries. Phospholipid is an essentialconstituent of cell membranes. Cholesterol is also an essentialconstituent of cell membranes, particularly in the nervous system.Cholesterol is also the principle precursor of cortisone and sexhormones. 93% of cholesterol is found in cells and only 7% in plasma.

Compositions

The compositions of the present invention are useful for the preventionand treatment of dysfunctional cardiovascular conditions in subjects inneed thereof, and contain electro-activated solutions of inorganic saltsand anti-oxidants with a stable negative oxidation-reduction potential(ORP) in a range between −50 mV and −500 mV, a conductivity between 11and 15 mS/cm and a pH in the range between 6.5 and 7.6.

The stable compositions of the invention are prepared by mixing twoelectro-activated solutions, Solution A with a stable negativeoxidation-reduction potential, and Solution B with a stable positiveoxidation-reduction potential, immediately prior to use.

The electro-activated solutions with a stable positive or negativeoxidation-reduction potential may be obtained by exposing an aqueoussalt solution to electric current. The electric currentelectro-activates the molecules, atoms and ions in the solution and theions are redistributed in the electric field. As a result, the aqueoussolution in the cathode chamber (catholyte) is charged with a negativeORP and acquires bio-regenerative properties. The aqueous solution inthe anode chamber (anolyte) is charged with a positive ORP and acquiresantiseptic properties.

The electro-activated solutions with a stable positive or negativeoxidation-reduction potential may be prepared by any method known in theart. Preferably, sterile, purified water is electro-activated using anopen plate palladium-coated electrode in a ceramic-type housing of amodule containing ferrous and non-ferrous alloys capable of imparting afixed magnetic field of at least 7.5 Gauss over a period of time of atleast 1.75 minutes at a flow rate of at least 0.75 liter/minute. Theelectro-activated water thus obtained, which has an initial positiveoxidation-reduction potential (ORP) in a range between +700 mV and +900mV, is then collected in a sterilized, air-free and endotoxin-freevessel and used to prepare Solution A and Solution B. Both solutions areused as a diluent for vitamins, salts and minerals.

Solution A is prepared by adding 2-diethylaminoaceto xylidide to thevessel filled with the electro-activated water until completedissolution; adding ascorbic acid or sodium ascorbate, which are bothstrong anti-oxidants, in a concentration of 83.6-95.5 g/L and 90.0-100.0g/L, respectively, to reach a stable, negative ORP in a range between−500 mV and −900 mV and stirring until dissolved; adding salts, vitaminand minerals and lastly cyanocobalamin to reach a pH between 3.2 and4.5; and bubbling nitrogen through the mixture.

In a specific embodiment, 1.0 liter of Solution A contains the followingvitamins, salts and minerals:

Ascorbic acid 83.6-95.5 g/L

Magnesium Sulphate hexahydrate 57.1-64-7 g/L

2-diethylaminoaceto,xylidide 28.5-32.3 g/L

Niacinamide 9.4-10.6 g/L

Pyridoxin HCL 9.4-10.6 g/L

Riboflavin-5-phosphate sodium 0.18-029 g/L

Thiamin HCL 5.7-6.5 g/L

Cyanocobalamin crystalline 0.17-0.2 g/L

Electrochemically activated water+ 997.50 ml

To prepare Solution B, sodium bicarbonate, sodium chloride, a saltselected from magnesium sulfate and magnesium chloride and optionallycalcium are added to the vessel filled with the electro-activated wateruntil complete dissolution. The solutes increase ionization and producea stably charged anti-inflammatory solution. A stabilizer may be alsoadded to the solution in an amount of 0.5% mass/volume to increaseconductive ionization and produce a stably charged solution with astable, positive oxidation-reduction potential in a range between +500mV and +900 mV and a pH between 6.5 and 7.8. The stabilizer may be mixedinto the solution by agitation or a sonicator bath and the solution isimmediately sealed to prevent entry of oxygen.

In a specific embodiment, 1.0 liter of Solution B contains the followingsalts and minerals:

Sodium Bicarbonate USP 82.4-93.2 g/L

Magnesium Sulphate hexahydrate 19.1-21.8 g/L

Electrochemically activated water+ 998.5 ml

Both solutions A and B are stable for a period of at least 12 monthswhen stored at 15°-25° C. in no direct sunlight.

Solution A and Solution B are then mixed prior to administration toproduce a composition with a stable negative oxidation-reductionpotential (ORP) in a range between −50 mV and −500 mV, a conductivitybetween 11 and 15 mS/cm and a pH in the range between 6.5 and 7.6. In apreferred embodiment, the stable composition comprises 0.5-10% magnesiumsulfate hexahydrate, 5.0-20.0% ascorbic acid, 0.2-2.0% niacinamide,0.2-2% pyridoxine HCl, 0.01-2.0% calcium D pantothenate, 0.1-1.0%thiamin HCl, 0.01-0.1% riboflavin, 0.001-0.1% cyanocobalamin, 0.05-10%sodium lactate and 5-500 ml magnetic dipole stabilized water. Thecomposition thus produced is stable for at least 48 hours when stored at4°-8° C., and may be administered as is or diluted in isotonicintravenous (IV) fluid.

The present inventors unexpectedly discovered that the electro-activatedsolutions of the invention have high anti-oxidant properties. Inparticular, the inventors unexpectedly found that parenteraladministration of the electro-activated solutions to a subject with orat risk of developing a dysfunctional cardiovascular condition preventsor eliminates the cardiovascular condition. Without being bound to anytheory, it is believed that the solutions of the invention improveoxygen delivery to the arteries, veins and cardiac muscle and thetransport of anti-oxidants and minerals to the bloodstream by causingchanges in the concentration gradient of the cellular membranes which inturn modulate transport of physiological ions, such as sodium andpotassium. In addition, it is believed that the electro-activatedsolution of the invention improves membrane permeability and thusincreases the rate of transport of the minerals and anti-oxidants in thesolution. Furthermore, parenteral injection of the composition into thebloodstream provides for the fast and prompt reaching of high levels ofnutrients, anti-oxidants and minerals in the blood, thus eliminating theneed for digestive enzymes and providing an antidote to conditionscaused by cardiovascular dysfunctions.

The compositions of the invention are added to isotonic intravenous (IV)fluid and parenterally administered to the subject by intravenousinjection, intra-arterial injection, or by intravenous andintra-arterial injection. Following treatment, the composition may beadministered periodically as a maintenance therapy. Typically, whenadministered by intravenous injection, the composition is administeredin an amount of 50-300 ml daily, biweekly, weekly, bimonthly or monthlyfor a period from 14 days to six months, and when administered byintra-arterial injection, the composition is administered in an amountof 10-50 ml daily, biweekly, weekly, bimonthly or monthly for a periodfrom 14 days to six months.

The treatment envisioned by the invention can be used for subjects witha pre-existing condition, or for subjects pre-disposed to acardiovascular disease or dysfunction.

EXAMPLES Example 1 Preparation of Electro-Activated Solution

An electro-activated aqueous solution is prepared using an open platepalladium-coated electrode in a ceramic-type housing of a modulecontaining ferrous and non-ferrous alloys capable of imparting a fixedmagnetic field of at least 7.5 Gauss over a period of time of at least1.75 minutes at a flow rate of at least 0.75 liter/minute. Theelectro-activated water thus obtained, which has an initial positiveoxidation-reduction potential (ORP) in a range between +700 mV and +900mV, is then collected in a sterilized, air-free and endotoxin-freevessel and used as a diluent for vitamins, salts and minerals. Theelectro-activated water thus obtained, which has an initial positiveoxidation-reduction potential (ORP) in a range between +700 mV and +900mV, is then collected in a sterilized, air-free and endotoxin-freevessel and used to prepare Solution A and Solution B. Both solutions areused as a diluent for vitamins, salts and minerals.

Solution A is prepared by adding 2-diethylaminoaceto xylidide to thevessel filled with the electro-activated water until completedissolution; adding ascorbic acid or sodium ascorbate, which are bothstrong anti-oxidants, in a concentration of 83.6-95.5 g/L and 90.0-100.0g/L, respectively, to reach a stable, negative ORP in a range between−500 mV and −900 mV and stirring until dissolved; adding salts, vitaminand minerals and lastly cyanocobalamin to reach a pH between 3.2- and4.5; and bubbling nitrogen through the mixture.

In a specific embodiment, 1.0 liter of Solution A contains the followingvitamins, salts and minerals:

Ascorbic acid 83.6-95.5 g/L

Magnesium Sulphate hexahydrate 57.1-64-7 g/L

2-diethylaminoaceto,xylidide 28.5-32.3 g/L

Niacinamide 9.4-10.6 g/L

Pyridoxin HCL 9.4-10.6 g/L

Riboflavin-5-phosphate sodium 0.18-029 g/L

Thiamin HCL 5.7-6.5 g/L

Cyanocobalamin crystalline 0.17-0.2 g/L

Electrochemically activated water+ 997.50 ml

To prepare Solution B, sodium bicarbonate, sodium chloride, a saltselected from magnesium sulfate and magnesium chloride and optionallycalcium are added to the vessel filled with the electro-activated wateruntil complete dissolution. The solutes increase ionization and producea stably charged anti-inflammatory solution. A stabilizer may be alsoadded to the solution in an amount of 0.5% mass/volume to increaseconductive ionization and produce a stably charged solution with astable, positive oxidation-reduction potential in a range between +500mV and +900 mV and a pH between 6.5 and 7.8. The stabilizer may be mixedinto the solution by agitation or a sonicator bath and the solution isimmediately sealed to prevent entry of oxygen.

In a specific embodiment, 1.0 liter of Solution B contains the followingsalts and minerals:

Sodium Bicarbonate USP 82.4-93.2 g/L

Magnesium Sulphate hexahydrate 19.1-21.8 g/L

Electrochemically activated water+ 998.5 ml

Both solutions A and B are stable for a period of at least 12 monthswhen stored at 15°-25° C. in no direct sunlight.

Solution A and Solution B are then mixed prior to administration toproduce a composition with a stable negative oxidation-reductionpotential (ORP) in a range between −50 mV and −500 mV, a stable pHbetween 6.5 and 7.6, and a conductivity in the range between 11 and 15mS/cm.

The final mixture thus obtained comprises the following ingredients:

Magnesium sulfate hexahydrate 0.5-10%

Sodium Bicarbonate 0.5-10%

Ascorbic Acid 5.0-20%

Niacinamide 0.2-2.0%

Pyridoxin HCl 0.005-0.2%

Calcium D Pantothenate 0.01-2.0%

Thiamin HCl 0.1-1.0%

Riboflavin 0.01-0.1%

Cyanocobalamin 0.001-0.1%

Magnetic Dipole Stabilized Water 5.0-500 ml

2-di-ethylaminoethanol 1.0-3.0%

Example 2 The Coronary Calcium Scan

The coronary calcium scan is a test that assists in showing whether apatient is at risk of developing a coronary artery disease (CAD), bydetermining the presence of plaque (fatty deposits) in blood vessels.The presence and amount of calcium detected in a coronary arteryindicates the presence and amount of atherosclerotic plaque. Sincecalcium deposits appear years before the development of heart diseasesymptoms such as chest pain and shortness of breath, a coronary calciumscan is most useful for people who are at moderate risk of having aheart attack within the next 10 years, and may help doctors decidewhether a patient needs treatment. The calcified plaque burden caused bycalcium deposits is measured with the Calcium Score, also called theAgatston Calcium Score, which is computed for each of the coronaryarteries based upon the volume and density of the calcium deposits. Thecalcified plaque burden does not correspond directly to the percentageof narrowing in the artery but does correlate with the severity of theunderlying coronary atherosclerosis. The score is then used to determinethe calcium percentile, which compares the calcified plaque burden in asubject to the calcified plaque burden in other asymptomatic men andwomen of the same age. The calcium score, in combination with thepercentile, enables the physician to determine the risk of developingsymptomatic coronary artery disease and to measure the progression ofdisease and the effectiveness of treatment.

A score of zero indicates the absence of calcified plaque burden andsignificant coronary artery narrowing, although it does not entirelyrule out the presence of soft, non-calcified plaque or the possibilityof a cardiac event. A subject with a score of zero has a very lowlikelihood of a cardiac event over at least the next 3 years. A scoregreater than zero indicates at least some coronary artery disease. Asthe score increases, so does the likelihood of a significant coronarynarrowing and coronary event over the next 3 years, compared to peoplewith lower scores. Similarly, the likelihood of a coronary eventincreases with increasing calcium percentiles. Table 1 below shows therelation between the calcium score and the risk of coronary arterydisease.

TABLE 1 Risk of Coronary Calcium Score Implication Artery Disease 0 Noidentifiable plaque Very low, generally less than 5% 1-10 Minimalidentifiable plaque Very unlikely, less than 10% 11-100 Definite, atleast mild Mild or minimal atherosclerotic plaque coronary narrowingslikely 101-400 Definite, at least moderate Mild coronary arteryatherosclerotic plaque disease highly likely, significant narrowingspossible 401 or higher Extensive atherosclerotic plaque High likelihoodof at least one significant coronary narrowing

Example 3 The Calcium Plaque Burden of a Subject with a High CalciumScore

The plaque burden of a 45 years old male with a family history ofhypertension and diabetes mellitus type 2 and an Agatston calcium scoreof 467 was determined. The calcium score was 17 in the left maincoronary artery, 20 in the right coronary artery, 264 in the leftanterior descending coronary artery, 166 in the circumflex artery and 0in the posterior descending artery. The high calcium score indicatesthat the subject has a very high risk of coronary artery disease. Theplaque burden data are shown in Table 2 below.

TABLE 2 Calcium Plaque Burden of a patient with a score of 467 VolumeCalcium Score Region (mm3) (Agatston) Left Main 26 17 Right CoronaryArtery 38 20 Left Anterior Descending 251 264 Circumflex 145 166Posterior Descending 0 0 Artery Other 1 0 0 Other 2 0 0 Other 3 0 0Total 460 467

Example 4 Treatment of Subjects with the Electro-Activated Solution

Twenty male and female individuals between the ages of 24 and 63 wererandomly selected for the treatment, based on age, physical activity andbody mass index (BMI). Subjects with a family history of cardiovasculardiseases, diabetes mellitus or cancer were included in the treatment.The individuals were subjected to a complete physical examination, bloodand urine analyses, calcium score measurement and radiologicalexamination. The calcium score was 0 in nine subjects; 1 in one subject;24 in two subjects; 32 in one subject; 40 in one subject; 42 in onesubject; 46 in one subject; 57 in one subject; 155 in one subject; 482in one subject; and 1668 in one subject. The radiological studyperformed on the twenty individuals showed that individuals with acalcium score of 0 had no calcified plaques, whereas subjects with acalcium score between 24 and 57 had calcified plaques in the leftanterior descending artery (LAD) and were at mild risk for coronaryartery diseases. Subjects with a calcium score of 155 or 482 showedcalcification in the right coronary artery (RCA) and left anteriordescending artery (LAD) with a definite risk for coronary arterydisease. The patient with a calcium score of 1668 showed calcificationof the right coronary artery, left main artery, left anterior descendingartery (LAD), the diagonal and circumflex arteries, confirming a veryhigh risk for coronary artery diseases.

All subjects had their blood pressure and pulse taken before and aftereach treatment session and treated with an electro-activated solutionprepared as in Example 1. The solution was administered to each subjectby intravenous injection in an amount of 100 ml of sterile diluent (0.9%sodium chloride injection) for 35 to 55 minutes once or twice a week fora period ranging from two weeks to two months.

At the end of the treatment, all subjects reported feeling extremelywell and energetic, improvement in sleeping patterns and mentalalertness and a decrease in anxiety and stress level. Several subjectsreported an improvement in visual, hearing and sensory acuity and anincrease in hair growth. A few subjects reported increased libido anddecrease in weight. Some subjects reported the beneficial sensation ofhot flushes and tingling in the extremities. One subject reported animprovement in pre-menstrual symptoms. One obese subject whose ankleswere dark blue because of the excessive weight, reported that the ankleshad turned pink after the fourth treatment. The smokers in the groupreported a decrease in nicotine intake at the end of treatment. Asubject suffering from angina attacks before treatment reported adecrease in chest pains after beginning of treatment. No side effectswere reported.

Example 5 The Effect of the Treatment on the Calcium Score

The calcium score was measured in the individuals subjected to thetreatment with the electro-activated solution at the end of treatment.Table 3 below shows the calcium score of nine individuals with aninitial medium to high calcium score before and after 12 treatmentsessions. The data in Table 3 clearly show a positive effect of thetreatment on individuals with an initial calcium score of 46 and above.

TABLE 3 Calcium Score Calcium Score Percentage of Before After 12Increase or Patient Treatment Treatment Sessions Decrease 1 24 25  4%Increase 2 24 26  8% Increase 3 32 31  3% Decrease 4 40 42  5% Increase5 46 29 37% Decrease 6 57 40 29% Decrease 7 155 121 22% Decrease 8 482441  9% Decrease 9 1668 1539  8% Decrease

Example 6 Treatment of Patients with Angina

Patients A and B are diagnosed with stable angina. Patient A is treatedwith conventional medications, including heparin, aspirin and betablocker. Patient B is administered the electro-activated solutionprepared as in Example 1 by intravenous injection in an amount of 200ml/day for 30 days.

After one month of treatment both patients are examined. Patient A,after a brief period of remission, shows symptoms of angina. Patient B,treated according to the method of the invention, shows completeremission and symptoms of angina have not reappeared after one year.

Example 7 Treatment of Patients with Buerger's Disease

The effect of the method of treatment according to the invention isstudied on subjects with Buerger's Disease. 18 heavy-smoker malesbetween the ages of 20 and 40 and 5 women over the age of 50 arediagnosed with Buerger's Disease. Symptoms include intense pain in theextremities (claudication), numbness and/or tingling in the limbs, skinulcerations and gangrene. 8 subjects show signs of Raynaud's disease, aphenomenon in which the distal extremities turn white upon exposure tocold. Angiograms of all patients demonstrate lack of blood flow to thevessels of the hand. An electro-activated solution prepared as inExample 1 is administered to each subject by intravenous injection in anamount of 200 ml/day for 20 days. Within 15 days from the beginning oftreatment, the symptoms of Buerger's Disease disappear and angiogramsshow net improvement in blood flow.

What is claimed is:
 1. A stable therapeutic composition comprising anelectro-activated solution, wherein the electro-activated solution hasan oxidation-reduction potential (ORP) in the range between −500 mV and−900 mV for a period of at least 12 months and a pH in the range between3.2 and 4.5, and the composition comprises: Ascorbic acid 83.6-95.5 g/L;Magnesium Sulphate hexahydrate 57.1-64.7 g/L;2-diethylaminoaceto,xylidide 31.5-37.5 g/L; Niacinamide 9.4-10.7 g/L;Pyridoxin HCL 9.4-10.7 g/L; Riboflavin-5-phosphate sodium 0.18-0.2 g/L;Thiamin HCL 5.75-6.5 g/L; Cyanocobalamin crystalline 0.17-0.2 g/L; andElectrochemically activated water+.